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Beyond Structural Stability: Ongoing Electrical Remodeling in ATTR-CM Treated With Tafamidis
Session:
Sessão de Posters 12 - Estratégias terapêuticas e desfechos em vida real na ATTR-CM
Speaker:
Rita Ventura
Congress:
CPC 2026
Topic:
L. Cardiovascular Pharmacology
Theme:
31. Pharmacology and Pharmacotherapy
Subtheme:
31.1 Cardiovascular Pharmacotherapy
Session Type:
Posters Eletrónicos
FP Number:
---
Authors:
Rita Ventura; Inês Brito e Cruz; Maria João Primo; Didier Martinez; Vanessa Lopes; João Rosa; Manuel Oliveira Santos; Maria João Ferreira; Lino Gonçalves
Abstract
<p><strong>Introduction: </strong>Tafamidis improves survival in transthyretin cardiac amyloidosis (ATTR-CM),</p> <p>but detailed real-world characterization of its longitudinal clinical, electrical, and structural</p> <p>effects remains limited. Clarifying disease progression under tafamidis in routine care is</p> <p>essential.</p> <p><strong>Purpose:</strong> To describe 12-month changes in functional status, biomarkers, ECG parameters,</p> <p>and echocardiographic structure/function in patients with ATTR-CM treated with tafamidis.</p> <p><strong>Methods: </strong>Retrospective observational study of patients with ATTR-CM treated with tafamidis.</p> <p>NYHA class, NT-proBNP, ECG variables (PR interval, QRS duration, QRS voltage pattern,</p> <p>new-onset atrial fibrillation), and echocardiographic parameters (wall thickness, LVEF, GLS,</p> <p>diastolic indices, and LA volume index) were assessed at baseline and 12 months.</p> <p><strong>Results: </strong>Forty-five patients initiated tafamidis (median age 83 years; 80% male).</p> <p>Hypertension (88.9%) and atrial fibrillation (AF) (60%) were frequent; 22.2% had prior</p> <p>pacemaker implantation. Population baseline finding included mild functional impairment,</p> <p>elevated NT-proBNP, prolonged QRS duration, and typical structural findings.</p> <p>NYHA class remained stable (median Δ 0.0 [–1.0 to 0.0], p = 0.491), though 35.7% improved.</p> <p>NT-proBNP showed marked inter-individual variability without a consistent trend (median Δ</p> <p>+376 pg/mL [−1332 to +750], p = 0.807).</p> <p>Electrically, PR interval remained stable (median Δ +4 ms [−38 to +19], p = 0.866), while QRS</p> <p>duration increased significantly (Δ +7 ms [3.5 to 17.8], p = < 0.001).</p> <p>Despite tafamidis therapy, new-onset AF emerged in 32% of previously non-AF patients.</p> <p>Echocardiographic parameters remained largely unchanged: LVEF (Δ −2.0% [−7.0 to +3.0], p</p> <p>= 0.363), septal thickness (Δ 0.0 mm [−1.0 to 0.5], p = 0.518), posterior wall thickness (Δ +1.0</p> <p>mm [−2.77 to +1.85], p = 0.916), LV mass index (Δ +2.7 g/m² [−40.6 to 19.4], p = 0.893), GLS</p> <p>(Δ +2.6% [−2.16 to +9.60], p = 0.500), E/e′ (Δ +3 [−5.75 to +5], p = 0.713), and LA volume</p> <p>index (Δ +3 mL/m² [−1.5 to 13.5], p = 0.195).</p> <p><strong>Conclusion: </strong>Tafamidis stabilizes structural, functional, and biomarker profiles in real-world</p> <p>ATTR-CM, but electrical disease continues to progress, with significant QRS widening and</p> <p>frequent new-onset AF. These findings highlight persistent electrophysiological vulnerability</p> <p>and support routine ECG monitoring, as well as validation in larger cohorts.</p>
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